Stimulation of basolateral Na(+)-HCO3- cotransporter by angiotensin II in rabbit renal cortex.

Angiotensin (ANG) II is now recognized as a powerful direct controller of Na+ reabsorption in the proximal convoluted tubule, a property that predominantly reflects stimulation of the transepithelial NaHCO3 flux. Numerous studies have established that this effect of ANG II represents stimulation of the apical Na+/H+ exchanger, but a single microperfusion study has also suggested direct stimulation of the basolateral Na(+)-HCO3- cotransporter. We have carried out studies in basolateral membrane vesicles from rabbit renal cortex to examine directly whether ANG II exerts an independent effect on the Na(+)-HCO3- cotransporter.

Endothelin-1 stimulates the Na+/H+ and Na+/HCO3- transporters in rabbit renal cortex.

Endothelin-1 (ET-1) is the most potent endogenous vasoconstrictor identified to date, raising the strong possibility of its involvement in the pathogenesis of systemic hypertension. Whether ET-1 exerts a direct stimulating effect on sodium reabsorption in the renal proximal convoluted tubule, the dominant locus of sodium reabsorption in the nephron, is currently unknown. Such an effect would suggest yet another mechanism by which ET-1 might mediate systemic hypertension.

Effect of sulfhydryl compounds on ATP-stimulated H+ transport and Cl- uptake in rabbit renal cortical endosomes.

The vacuolar H+ ATPase is inhibited by N-ethylmaleimide (NEM), a sulfhydryl compound, suggesting the involvement of a sulfhydryl group in this transport process. We have examined the effects of several sulfhydryl-containing compounds on the vacuolar H+. ATPase of rabbit renal cortical endosomes.

Na(+)-H+ exchange, but not Na(+)-K(+)-ATPase, is present in endosome-enriched microsomes from rabbit renal cortex.

Previous studies have demonstrated a Na(+)-dependent decrease in the ATP-generated acidification of endosomes and have attributed it to the presence of either a Na(+)-H+ exchanger or a Na(+)-K(+)-adenosinetriphosphatase (ATPase) in parallel with the vacuolar H(+)-ATPase. In the present study we have examined the possibility that both of these two Na+ transporters might be present in endosome-enriched microsomes isolated from rabbit renal cortex. After the establishment of a stable pH gradient by ATP in this preparation, addition of Na+ induced a decrease in the pH gradient.